Patients with NRG1-rearranged tumors may be more sensitive to therapies targeting ERBB3 than ERBB2, and the presence of NRG1 fusions in multiple tumor types supports a basket trial approach to evaluate ERBB3 inhibitors.

EGFR amplifications were identified in 5% of patients with gastroesophageal adenocarcinoma, and anti-EGFR therapy achieved responses in 4 of 7 patients with EGFR amplification, although various resistance mechanisms emerged.

The spectrum of ALK resistance mutations to the third-generation ALK inhibitor lorlatinib were identified by an in vitro mutagenesis screen and in clinical specimens from patients with ALK-positive lung cancer.

Analysis of 1,211 colorectal tumors found that MSI-H tumors have a higher frequency of mutations associated with immunoediting and both MSI-H and non-hypermutated tumors have WNT activating mutations that promote immune exclusion.